Several studies have domonstrated reductions in vascular events with Antiplatelet agents in patients with unstable angina, prior MI, or prior stroke/TIA. Platelet activation induces a calcium-dependent conversion of the platelet glycoprotein (GP) IIb/IIIa complex into a receptor for fibrinogen or von Willebrand factor (vWF). The conversion fo the GPIIb/IIIa complex into a binding site for fibrinogen and vWF appears to be the final common pathway for all physiologic mediators of platelet aggregation. An inhibitor of this pathway is therefore likely to be an effective therapeutic agent. This hypothesis has been evaluated in patients undergoing percutaneous transluminal coronary angioplasty (PTCA) using intravenously administered monoclonal antibodies directed against the platelet GPIIb/IIIa complex, or peptide, or nonpeptide receptor antagonists. It has been hypothesized that longer term GPIIb/IIIa inhibition, such as achievable with an oral agent, should sustain the benefit provided by acute administration of an intravenous agent, and should represent an advance over therapy with less potent agents, such as aspirin. DMP 754 is an investigational GPIIb/IIIa inhibitor drug currently being evaulated in Phase I/II studies. DMP 754 is an orally administered methylester prodrug requiring in vivo hydrolysis by esterases to XV459 which is a potent and selective GP IIb/IIIa receptor antagonist. The primary objective of this study is to investigate the effects and dose-relationship of daily administration of DMP 754 vs. placebo on inhibition of platelet aggregation (IPA) in aspirin-treated patients over a 27-day period following PTCA.